ArticlePLoS pathogens2014
Toxoplasma gondii profilin promotes recruitment of Ly6Chi CCR2+ inflammatory monocytes that can confer resistance to bacterial infection.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- CX3CR1 and CCR2: dynamic myeloid cell states across inflammatory diseases with implications for oral health and disease.Frontiers in immunology · 2026Review
- Toxoplasma gondii soluble antigen (STAg) induces resistance against Mycobacterium tuberculosis in a human monocyte cell line via P2X7 receptor.Molecular biology reports · 2025Article
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- Parasite-induced IFN-γ regulates host defense via CD115 and mTOR-dependent mechanism of tissue-resident macrophage death.PLoS pathogens · 2024Article
- Deficiency in astrocyte CCL2 production reduces neuroimmune control of Toxoplasma gondii infection.PLoS pathogens · 2024Article
- Immunotoxicity Evaluation of Trihalophenolic Disinfection By-Products in Mouse and Human Mononuclear Macrophage Systems: The Role of RNA Epitranscriptomic Modification in Mammalian Immunity.Environmental health perspectives · 2023Article
- Article
- Dual Transcriptomics To Determine Gamma Interferon-Independent Host Response to Intestinal Cryptosporidium parvum Infection.Infection and immunity · 2022Article
- Novel Murine Pancreatic Tumor Model Demonstrates Immunotherapeutic Control of Tumor Progression by a Toxoplasma gondii Protein.Infection and immunity · 2021Article
- ChronicProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Monocyte dysregulation: consequences for hepatic infections.Seminars in immunopathology · 2021Review
- Aging with Toxoplasma gondii results in pathogen clearance, resolution of inflammation, and minimal consequences to learning and memory.Scientific reports · 2020Article
- Perivascular localization of macrophages in the intestinal mucosa is regulated by Nr4a1 and the microbiome.Nature communications · 2020Article
- TLR11-independent inflammasome activation is critical for CD4+ T cell-derived IFN-γ production and host resistance to Toxoplasma gondii.PLoS pathogens · 2019Article
- Transcriptional Analysis Shows a Robust Host Response toInfection and immunity · 2019Article
- Long-Term Impact ofFrontiers in cellular and infection microbiology · 2019Article
- Alarmin S100A11 initiates a chemokine response to the human pathogen Toxoplasma gondii.Nature immunology · 2019Article
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- Hepatic recruitment of CD11b+Ly6C+ inflammatory monocytes promotes hepatic ischemia/reperfusion injury.International journal of molecular medicine · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ly6C+ inflammatory monocytes are essential to host defense against Toxoplasma gondii, Listeria monocytogenes and other infections. During T. gondii infection impaired inflammatory monocyte emigration results in severe inflammation and failure to control parasite replication. However, the T. gondii factors that elicit these monocytes are unknown. Early studies from the Remington laboratory showed that mice with a chronic T. gondii infection survive lethal co-infections with unrelated pathogens, including L. monocytogenes, but a mechanistic analysis was not performed. Here we report that this enhanced survival against L. monocytogenes is due to early reduction of bacterial burdens and elicitation of Ly6C+ inflammatory monocytes. We demonstrate that a single TLR11/TLR12 ligand profilin (TgPRF) was sufficient to reduce bacterial burdens similar to T. gondii chronic infection. Stimulation with TgPRF was also sufficient to enhance animal survival when administered either pre- or post-Listeria infection. The ability of TgPRF to reduce L. monocytogenes burdens was dependent on TLR11 and required IFN-γ but was not dependent on IL-12 signaling. TgPRF induced rapid production of MCP-1 and resulted in trafficking of Ly6Chi CCR2+ inflammatory monocytes and Ly6G+ neutrophils into the blood and spleen. Stimulation with TgPRF reduced L. monocytogenes burdens in mice depleted with the Ly6G specific MAb 1A8, but not in Ly6C/Ly6G specific RB6-8C5 depleted or CCR2-/- mice, indicating that only inflammatory monocytes are required for TgPRF-induced reduction in bacterial burdens. These results demonstrate that stimulation of TLR11 by TgPRF is a mechanism to promote the emigration of Ly6Chi CCR2+ monocytes, and that TgPRF recruited inflammatory monocytes can provide an immunological benefit against an unrelated pathogen.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.